Mayyas Fadia
Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, Yarmouk University, P.O. Box 566, Irbid, 21163 Jordan.
Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan.
J Diabetes Metab Disord. 2024 Dec 16;24(1):12. doi: 10.1007/s40200-024-01514-3. eCollection 2025 Jun.
Diabetes mellitus (DM) contributes to the development and progression of nephropathy and kidney diseases. Statins are known to have anti-inflammatory and antifibrotic effects. We aimed to test the short-term effect of atorvastatin on renal biomarkers of oxidative damage, inflammation, and fibrosis in a rat model of streptozotocin-induced DM.
Wistar rats were divided into; control rats, rats treated with atorvastatin (Ator, oral 40 mg/kg for 6 weeks), DM rats (DM, one intraperitoneal 40 mg/kg streptozotocin), and atorvastatin-treated DM rats (DM + Ator). Renal oxidative stress markers, inflammatory and mitogenic factors were measured.
Streptozotocin induced an increase in serum glucose, blood urea nitrogen, and creatinine levels. A marked increase in kidney to body weight ratio was found in DM groups. Diabetes resulted in an elevation in inflammatory biomarkers of galectin-3 and endothelin-1. Hyperglycemia induced an increase in lipid peroxides and a decrease in the superoxide dismutase (SOD) antioxidant level in the DM group. A significant increase in the fibrotic factor platelet derived factor-BB (PDGF-BB) expression was documented in the DM group. Six weeks use of atorvastatin normalized kidney endothelin-1, galectin-3, and the PDGF-BB, and attenuated the increase in lipid peroxides and the reduction in SOD levels.
Our findings suggest that short-term use of atorvastatin may attenuate the substrates for diabetic nephropathy via partial decrease of renal markers of inflammation, oxidative stress, and fibrosis.
糖尿病（DM）会促进肾病和肾脏疾病的发生与发展。已知他汀类药物具有抗炎和抗纤维化作用。我们旨在测试阿托伐他汀对链脲佐菌素诱导的糖尿病大鼠模型中肾脏氧化损伤、炎症和纤维化生物标志物的短期影响。
将Wistar大鼠分为：对照大鼠、接受阿托伐他汀治疗的大鼠（阿托伐他汀，口服40mg/kg，持续6周）、糖尿病大鼠（糖尿病组，腹腔注射40mg/kg链脲佐菌素）以及接受阿托伐他汀治疗的糖尿病大鼠（糖尿病+阿托伐他汀组）。检测肾脏氧化应激标志物、炎症和促有丝分裂因子。
链脲佐菌素导致血清葡萄糖、血尿素氮和肌酐水平升高。糖尿病组大鼠肾脏与体重之比显著增加。糖尿病导致半乳糖凝集素-3和内皮素-1等炎症生物标志物升高。高血糖导致糖尿病组脂质过氧化物增加，超氧化物歧化酶（SOD）抗氧化水平降低。糖尿病组纤维化因子血小板衍生生长因子-BB（PDGF-BB）表达显著增加。使用阿托伐他汀6周可使肾脏内皮素-1、半乳糖凝集素-3和PDGF-BB恢复正常，并减轻脂质过氧化物的增加和SOD水平的降低。
我们的研究结果表明，短期使用阿托伐他汀可能通过部分降低肾脏炎症、氧化应激和纤维化标志物来减轻糖尿病肾病的发病基础。
